The risk of becoming overweight is increased significantly if your family members are also overweight. Studies for example show that the offspring of two lean parents are less likely to be overweight than the offspring of overweight individuals. Of course, it could be argued that the reason that for this is genetic in origin, and to some extent this may be true. However, the increased risk of obesity could be due to the lifestyle habits passed from one generation to the other and therefore could be argued to be environmental in origin. Researchers have assessed the risk of being obese based on the number of existing family members who are obese in order to determine if it is possible to predict fatness in an individual. For example in one study1 researchers calculated that the risk of obesity for an individual in a family of four was well below the mean at 13 %, if the remaining family members were all lean. However, the risk increased significantly to 41 % if the remaining family members were all obese.
Interestingly though, group analysis showed that the risk of obesity for a father in a lean family was only 7 %, while the risk of obesity for a child in a lean family was only 4 %. However, for mothers, the risk of obesity in a lean family was much higher at 25 %. The authors explained this observation as resulting from socioeconomic status. In this respect they referred to data that showed that obese mothers in lean families were particularly prevalent in the lowest two socioeconomic groups. Therefore while the fatness of an individuals can be predicted from the fatness of the remaining family members, a correction has to be made for the position within the family in order to find the true risk. The authors concluded that obesity follows family lines and that the obese tend to replicate themselves in obesity. Predicting the risk of obesity is therefore relatively straight forward, however its causes are not so easy to explain as the results likely represent a mixture of both genetic and environmental factors.
However, while it could be argued that genetic factors influence obesity, the way in which this happens could be subtle. While defects in metabolism might explain obesity risk in some individuals, could genetic differences that affect feeding behaviour also be responsible for altering the risk of becoming overweight? One group of researchers2 investigated the eating habits of twins with a mean age of 40 years using identical (monozygotic) and fraternal (non-identical) twins. The aim of the study was to see if their genetic make-up influenced similarities in eating behaviour. The results showed that the diets of the identical twins pairs was significantly more similar than those of the non-identical twin pairs for protein and carbohydrate intakes. The authors concluded that the results provide evidence that in free living humans, genetic factors influence food selection. It is therefore likely that this in turn influences weight gain and obesity, if that selection is for lower quality obesogenic foods.
Dr Robert Barrington’s Nutritional Comments: Genes play a role in obesity. For example, ob/ob mice are genetically deficient in the hormone leptin and this causes them to become very fat. However, the numbers of individuals with with genetic conditions that influence weight gain is likely very low and this cannot explain the epidemic of obesity that has only manifest itself within the last few decades. The overriding influence on obesity for most individuals therefore would appear to be environmental in origin. The adoption of the Western diet by the affluent populations of the West mirrors the rise in the prevalence of obesity, and the association between poor quality diet and weight gain is well documented. Therefore although genes can influence weight gain through metabolic aberrations and through food selection bias, these mechanisms do not explain obesity when considering the timescales involved in its development in relation to adoption of the typical Western diet. We all have the power to control what we put in our mouths, and for most free will therefore likely determines the ultimate risk of becoming fat.
RdB
